0000000000114973

AUTHOR

Serafina Sciarrino

showing 7 related works from this author

Cigarette smoke alters IL-33 expression and release in airway epithelial cells

2014

AbstractAirway epithelium is a regulator of innate immune responses to a variety of insults including cigarette smoke. Cigarette smoke alters the expression and the activation of Toll Like Receptor 4 (TLR4), an innate immunity receptor. IL-33, an alarmin, increases innate immunity Th2 responses. The aims of this study were to explore whether mini-bronchoalveolar lavage (mini-BAL) or sera from smokers have altered concentrations of IL-33 and whether cigarette smoke extracts (CSE) alter both intracellular expression (mRNA and protein) and release of IL-33 in bronchial epithelial cells. The role of TLR4 in the expression of IL-33 was also explored.Mini-BALs, but not sera, from smokers show red…

Bronchial epithelial cellLipopolysaccharidesBlotting WesternBronchiInflammationRespiratory MucosaBiologyReal-Time Polymerase Chain ReactionBronchoalveolar LavageImmunoenzyme TechniquesBronchial epithelial cell; COPD; Cigarette smoke; IL-33; InflammationSmokeacute lung injury cigarette smokeinterleukin 33medicineCOPDHumansRNA MessengerReceptorMolecular BiologyCells CulturedCell ProliferationInflammationToll-like receptorInnate immune systemReverse Transcriptase Polymerase Chain ReactionInterleukinsCigarette smokeFlow CytometryInterleukin-33Immunity Innaterespiratory tract diseasesCell biologyToll-Like Receptor 4Interleukin 33ImmunologyIL-33TLR4Molecular MedicineRespiratory epitheliummedicine.symptomIntracellularBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Cigarette smoke increases BLT2 receptor functions in bronchial epithelial cells: in vitro and ex vivo evidence

2013

Summary Leukotriene B4 (LTB4) is a neutrophil chemotactic molecule with important involvement in the inflammatory responses of chronic obstructive pulmonary disease (COPD). Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke, the major risk factor for COPD. In this study we have explored whether cigarette smoke extracts (CSE) or soluble mediators present in distal lung fluid samples (mini-bronchoalveolar lavages) from smokers alter the expression of the LTB4 receptor 2 (BLT2) and peroxisome proliferator-activated receptor-α (PPAR-α) in bronchial epithelial cells. We also evaluated the effects of CSE on the expression of i…

Leukotriene B4NeutrophilsImmunologyIntercellular Adhesion Molecule-1Blotting WesternReceptors Leukotriene B4Peroxisome proliferator-activated receptorSettore MED/41 - AnestesiologiaInflammationBronchiBiologychronic obstructive pulmonary diseasechemistry.chemical_compoundTobaccoacute lung injiurybronchial epithelial cellleukotriene B4.medicineCell AdhesionImmunology and AllergyHumansPPAR alphaReceptorPromoter Regions GeneticCells Culturedchemistry.chemical_classificationInnate immune systemPlant Extractscigarette smokeSmokingEpithelial CellsOriginal Articlesrespiratory systemFlow CytometryIntercellular Adhesion Molecule-1Neutrophiliarespiratory tract diseasesacute lung injiury; bronchial epithelial cells; cigarette smoke; chronic obstructive pulmonary disease; inflammation; leukotriene B4.STAT1 Transcription FactorchemistryinflammationImmunologyRespiratory epitheliumRNA Interferencemedicine.symptomBronchoalveolar Lavage FluidProtein Binding
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Gamma enolase expression as early marker of neuronal differentiation of murine neuroblastoma cells N-115

2012

In this study we determined the levels of gamma enolase mRNA in mouse neuroblastoma cell line N-115 at early period of induction of differentiation by serum withdrawal. The expression of gamma enolase was examined by Northern blot analysis of total RNA extracted from cells induced for different lengths of time. We found a 3-fold increase in the level of gamma enolase mRNA after 24 hours of induction of differentiation and higher levels were detected in cells induced for longer time, reaching a 10-fold increase after four days.

Messenger RNAPeriod (gene)Clinical BiochemistryNeuronal differentiationBiomedical EngineeringBioengineeringCell BiologyMouse NeuroblastomaBiologyGamma-EnolaseMolecular biologyMurine neuroblastomaCell cultureNorthern blotBiotechnologyCytotechnology
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Novel alpha-galactosidase A mutation in a female with recurrent strokes.

2012

Abstract Anderson–Fabry disease (AFD) is an X-linked inborn error of glycosphingolipid catabolism resulting from the deficient activity of the lysosomal exoglycohydrolase, a-galactosidase A. The complete genomic and cDNA sequences of the human alpha-galactosidase A gene have been determined and to date, several disease-causing alpha-galactosidase A mutations have been identified, including missense mutations, small deletions/insertions, splice mutations, and large gene rearrangements We report a case of a 56-year-old woman with recurrent cryptogenic strokes. Ophthalmological examination revealed whorled opacities of the cornea (cornea verticillata) and dilated tortuous conjunctival vessels.…

Pathologymedicine.medical_specialtyHeterozygoteClinical BiochemistryMolecular Sequence DataMutation MissenseBiologymedicine.disease_causeExonRecurrencemedicineMissense mutationHumansCornea verticillataAmino Acid SequenceGeneMutationBase SequencePoint mutationGeneral MedicineSequence Analysis DNAMiddle Agedmedicine.diseaseFabry diseaseMolecular biologyAngiokeratomaPedigreeStrokealpha-GalactosidaseFabry DiseaseFemalemedicine.symptomClinical biochemistry
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Notch‐1 signaling activation sustains overexpression of interleukin 33 in the epithelium of nasal polyps

2019

Abstract BACKGROUND: Alterations in the nasal epithelial barrier homeostasis and increased interleukin 33 (IL-33) expression contribute to the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). AIMS: As Notch-1 signaling is crucial in repair processes of mucosa, the current study assessed Notch-1/Jagged-1 signaling and IL-33 in the epithelium of nasal polyps biopsies from allergic (A-CRSwNP; n = 9) and not allergic (NA-CRSwNP; n = 9) subjects by immunohistochemistry. We also assessed, in a model of nasal epithelial cells, the effects of stimulation of Notch-1 with Jagged-1 on the expression of IL-33 (by flow cytometry, immunofluorescence, and immunocytochemistry), Jagged-1 (…

AdultMale0301 basic medicineendocrine systemPhysiologyClinical BiochemistryImmunocytochemistryStimulationBiologyCell LineFlow cytometryYoung Adult03 medical and health sciencesNasal Polyps0302 clinical medicinestomatognathic systemmedicineHumansNasal polypsPhosphorylationReceptor Notch1SinusitisCyclic AMP Response Element-Binding ProteinNotch 1medicine.diagnostic_testEpithelial CellsCell BiologyMiddle AgedInterleukin-33medicine.diseaseRhinitis AllergicMolecular biologyEpitheliumUp-RegulationInterleukin 33Nasal Mucosa030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisChronic DiseaseIL-33; Notch-1; chronic rhinosinusitis; nasal epithelium; nasal polypsImmunohistochemistryFemaleNOTCH-1 INTERLEUKIN 33 NASAL POLYPSJagged-1 ProteinSignal TransductionJournal of Cellular Physiology
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Mutations in the GLA Gene and LysoGb3: Is It Really Anderson-Fabry Disease?

2018

Anderson-Fabry disease (FD) is a rare, progressive, multisystem storage disorder caused by the partial or total deficit of the lysosomal enzyme &alpha

0301 basic medicineProbandMaleDiseasemedicine.disease_causeSphingolipidCatalysilcsh:Chemistry0302 clinical medicineGla geneFabry disease; GLA gene; LysoGb3MedicineChildlcsh:QH301-705.5Spectroscopychemistry.chemical_classificationGeneticsAlleleAged 80 and overMutationComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineMiddle AgedPhenotype3. Good healthComputer Science ApplicationsPhenotypeChild PreschoolFemaleHumanAdultAdolescentGenotypeGlycolipidCatalysisArticleInorganic Chemistry03 medical and health sciencesYoung Adultotorhinolaryngologic diseasesHumansPhysical and Theoretical ChemistryMolecular BiologyGeneGLA geneAllelesAgedFabry diseaseSphingolipidsbusiness.industryOrganic ChemistryInfant NewbornLysoGb3InfantBiomarkerFabry disease; gla gene; lysogb3; adolescent; adult; aged; aged 80 and over; alleles; amino acid substitution; biomarkers; child; child preschool; fabry disease; female; genotype; glycolipids; humans; infant; infant newborn; male; middle aged; phenotype; sphingolipids; young adult; alpha-galactosidase; mutationmedicine.diseaseFabry disease030104 developmental biologyEnzymechemistrylcsh:Biology (General)lcsh:QD1-999Amino Acid Substitutionalpha-GalactosidaseMutationGlycolipidsbusiness030217 neurology & neurosurgeryBiomarkersInternational Journal of Molecular Sciences
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Ultrastructural evidence of collagenolytic activity in ductal infiltrating carcinoma of the human breast

1987

The stroma of ductal infiltrating carcinoma of the human breast shows characteristic and localized areas of collagen rarefaction and fragmentation. This finding has been correlated with a peculiar type of fibrillar damage, observed in a small percentage of collagen fibrils isolated in the native state from the tumour stroma. The same pattern of lesion has been reproduced in vitro by human collagenase digestion on reconstituted fibrils. No effect has been detected by other nonspecific proteases in the same system.

Cancer ResearchProteasesPathologymedicine.medical_specialtyMammary glandBreast Neoplasmsmacromolecular substancesBiologyLesionStromamedicineHumansTrypsinFragmentation (cell biology)AgedPancreatic ElastaseMiddle AgedIn vitroMicroscopy ElectronCarcinoma Intraductal NoninfiltratingMicrobial Collagenasemedicine.anatomical_structureOncologyCollagenaseUltrastructureFemaleCollagenmedicine.symptommedicine.drug
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